A new study by University of Miami (UM) scientists has discovered high concentrations of a compound called BMAA in shark fins, which is a neurotoxin linked to neurodegenerative diseases in humans, including Alzheimer’s and Lou Gehrig Disease (ALS). The study suggests that consumption of shark fin soup and cartilage pills may pose a significant health risk, in terms of degenerative brain diseases.
The Scale of the Slaughter
“Shark fins are primarily derived through finning, a practice whereby shark fins are removed at sea and the rest of the mutilated animal is thrown back in the water to die,” explains Dr. Neil Hammerschlag, research assistant professor of Marine Affairs & Policy and director of the RJ Dunlap Marine Conservation Program (RJD) at UM.
“Estimates suggest that fins from as many as 70 million sharks end up in soup annually. As a result, many shark species are on the road to extinction. Because sharks play important roles in maintaining balance in the oceans, not only is shark fin soup injurious to the marine environment, but our study suggests that it is likely harmful to the people who are consuming it.”
Seven species of shark were tested for this study: blacknose, blacktip, bonnethead, bull, great hammerhead, lemon, and nurse sharks, with samples being collected from live animals in waters throughout South Florida. These revealed high levels of a cyanobacterial neurotoxin called BMAA, which is believed to concentrate in the food chain.
“The quantities of BMAA in the samples are a cause for concern, not only with regard to shark fin soup, but also in terms of dietary supplements and other forms of shark products ingested by humans,” says study co-author Prof. Deborah Mash, Director of the UM Miami Brain Endowment Bank. The Bank supports basic and clinical research and holds one of the world’s largest collection of postmortem human brains encompassing a wide range of neurological disorders.
In 2009, Mash and her co-authors published a study demonstrating that patients dying with diagnoses of Alzheimer’s Disease and ALS had unusually high levels of BMAA in their brains, up to 256 ng/mg, whereas normal healthy aged people had no BMAA or only trace quantities of the toxin present. “BMAA was first linked to neurodegenerative diseases in Guam, which resulted in the progressive loss of structure and function of neurons.”
The shark study found a similar range and even higher BMAA in the fins tested, with levels of between 144 and 1836 ng/mg of BMAA, which overlapped with the levels measured in the brains of the Alzheimer’s and ALS victims. Coincidentally, this result fits with the BMAA levels in fruit bats examined by Paul Cox in Guam, animals which concentrate BMAA from their diet of cycad seeds. He linked the hunting and eating of fruit bats to the severe ALS/Parkinsonism dementia that afflicted local indigenous people.
“Not only does this new work provide important information on one probable route of human exposure to BMAA, it may lead to a lowering of the demand for shark fin soup and consumption of shark products, which will aid ocean conservation efforts,” added Hammerschlag.
The challenge now will be to use and communicate this research in the hope of lowering consumption of shark fin soup and other shark-based products throughout Asia, thereby helping to protect the sharks themselves.
Reference: Mondon, K., Hammerschlag, N., Basile, M., Pablo, J., Bannack, S.A. & Mash, D.C. Cyanobacterial Neurotoxin ß-N-Methylamino-L-alanine (BMAA) in Shark Fins Mar. Drugs 2012, 10(2), 509-520. The paper is available online here 10.3390/md10020509.